Human Immunodeficiency Virus

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Introduction. H.I.V. stands for ?Human Immunodeficiency Virus".A retrovirus (capable of converting RNA into DNA by Reverse transcriptase enzyme)Causes A.I.D.S. (Acquired Immune Deficiency Syndrome) in humans in which the immune system of the body fails leading to life threatening opportunistic i

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Human Immunodeficiency Virus

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1. “Human Immunodeficiency Virus” An Overview of etiology, A.I.D.S., Clinical presentation and Treatment Modalities

2. Introduction H.I.V. stands for “Human Immunodeficiency Virus”. A retrovirus (capable of converting RNA into DNA by Reverse transcriptase enzyme) Causes A.I.D.S. (Acquired Immune Deficiency Syndrome) in humans in which the immune system of the body fails leading to life threatening opportunistic infections and various un-usual tumors.

3. Introduction Discovered in 1984 and named HIV in 1986. First reported in young homosexual males but later found in non-homosexuals possibly by blood transfusion. HIV infects the Helper T (CD4) cells to which it binds

4. Types of H.I.V. Two types of HIV viruses exist:Type 1 and Type 2. Both types causes AIDS which is clinically indistinguishable from each other and are transmitted by the same routes (discussed later in presentation)

5. Epidemiology

6. Epidemiology 33 Million people till 2007 have AIDS worldwide 2.0 Million (20 Lack) people died of AIDS worldwide in 2007 There has been reduction in this disease in US and western Europe however in developing countries this disease is rising. In India only by 2006 were above 4 Million known cases of AIDS

7. Epidemiology According to WHO (2006) more than 25 Million people dead by AIDS since it's first recognition on December 1st 1981. More than 570,000 children in 2005 died of AIDS. In Africa more than 90 Million people are infected with HIV

9. Cells Targeted by HIV Three types of cells are targeted by HIV Virus. (a ) Helper T cells (specifically CD4+ T cells). (b )macrophages. and (c ) dendritic cells. Dendritic cells are the first cells encountered by HIV during sexual transmission when the virus is captured by dendritic cells in mucosa

11. Mechanism Of Action HIV enters macrophages and CD4+ T cells by the adsorption of glycoproteins on its surface to receptors on the target cell followed by fusion of the viral envelope with the cell membrane and the release of the HIV into the cell. Repeated replication takes place (by enzyme reverse transcriptase) infects multiple CD4 cells resulting in extremely low levels of these cells

12. Stages Of Disease Incubation period: asymptomatic, lasts between 2 and 4 weeks Acute infection: Lasts till 28 days . Symptoms: fever, lymphadenopathy, pharyngitis, rash, myalgia, malaise, mouth sores, headache, nausea & vomiting, enlarged liver/spleen, weight loss, thrush, and neurological symptoms. Latency Stage:Clinical latency can vary between two weeks and 20 years.Individuals who are in this phase are still infectious A.I.D.S.

13. Stages Of Disease

14. Stages Of Disease AIDS: Levels of CD4 Helper T cells fall below critical level. Life threatening opportunistic infections arise along with unusual tumors. First symptoms include unexplained weight loss, respiratory tract infections (sinusitis, pharyngitis,otitis media (middle ear infection) and pneumonia) Skin rashes and oral ulcerations appear.

15. Stages Of Disease Tumors include: Cerebral lymphoma,non-Hodgkin's lymphoma, Kaposi's sarcoma Pneumonia in this stage can be fatal Neurological problems such as encephalopathy, neuropathy,retinitis,dementia may be present in 50% of cases

16. Following oral manifestations may be seen in HIV infection: Thrush/Candidiasis (Pseudomembranous and erythematous) Angular cheilitis Dry mouth Oral pain Hairy leucoplakia

17. Herpes simplex virus infection Aphthous ulcer HIV associated periodontal diseases Linear gingival erythema

18. Group 1 : Lesions strongly associated with HIV infection Candidiasis (Erythematous& Pseudomembranous) Hairy leukoplakia Kaposi’s sarcoma Non-Hodgkin’s lymphoma Periodontal disease Linear gingival erythema Necrotizing (ulcerative) gingivitis Necrotizing (ulcerative) periodontitis Oral Lesions Associated With H.I.V.

19. Group 2 : Lesions less commonly associated with HIV infection Bacterial infections Mycobacterium avium-intercellulare Mycobacterium tuberculosis Melanotic hyperpigmentation Melanotic hyperpigmentation Necrotizing (ulcerative) stomatitis Salivary gland disease Dry mouth Viral infections Herpes simplex virus* Human papillomavirus (warty-like lesions) Condyloma acuminatum Focal epithelial hyperplasia Verruca vulgaris Oral Lesions Associated With H.I.V.

20. Group 3 : Lesions seen in HIV infection Bacterial infections Actinomyces israelii,Escherichia coli,Klebsiella pnuemoniae Cat-scratch disease Fungal infections other than candidiasis Cryptococcus neoformans Geotrichum candidum Histoplasma capsulatum* Aspergillus flavus Neurologic disturbances Facial palsy Trigeminal neuralgia Recurrent aphthous stomatitis*Viral infections Cytomegalovirus* Molluscum contagiosum Oral Lesions Associated With H.I.V.

21. HIV tests are used to detect the presence of the human immunodeficiency virus in serum, saliva, or urine. Such tests may detect HIV antibodies, antigens, or RNA. Tests employed are : ELISA (Enzyme Linked Immunosorbent Assay) Western Blot Rapid or point-of-care test Investigations

22. ELISA detects antibodies to HIV-1. Non-reactive to ELISA are HIV negative and reactive ELISA specimens undergoes confirmatory testing with a more specific supplemental tests (Western Blot) ELISA alone cannot be used to diagnose HIV positive case until confirmed by Western Blot In ELISA we take patient's serum and make HIV antibodies. If HIV is present in the serum, antibodies bind to HIV and a change in color takes place Investigations

23. In Western Blot, number of viral bands are indicative of result. If no bands present, then HIV negative If 1 brand present of 3 proteins of HIV ( GAG, POL, and ENV ) then HIV +ve. Polymerase Chain Reaction (PCR) . amplifies HIV DNA hence the amount of virus in the sample can be quantified with sufficient accuracy to detect changes. Rapid or point-of-care tests should be used in conjunction with the clinical status, history, and risk factors of the person being tested OraQuick is an antibody test that provides results in 20 minutes Clearview Complete HIV 1/2 and Clearview HIV 1/2 Stat-Pakprovide results within 15 minutes Investigations

24. The only known method of prevention is avoiding exposure to the virus. However, a course of antiretroviral treatment administered immediately after exposure, referred to as post-exposure prophylaxis, is believed to reduce the risk of infection if begun as quickly as possible. Anti-retroviral drugs such as :reverse transcriptase inhibitors (Zidovudine, Didanosine, Lamivdine), non-nucleoside reverse transcriptase inhibitors (Nevirapine, efavirens) and retroviral protease inhibitors (Indinavir, Ritonavir) are used currently. HAART (Highly Active Anti-retroviral Therapy) includes use of 3 or more drugs Treatment

25. Treatment of AIDS related oral disorders

26. References Peter C Hayes, Thomas W.Mackay, Ewan H.Forest, Roger A. Fisken.Churchill's Pocketbook of Medicine.In:Infectious Disease.3rd ed.London: Churchill Livingstone 2002:pp 285-9 Ramírez-Amador VA, Espinosa E, González-Ramírez I, Anaya-Saavedra G, Ormsby CE, Reyes-Terán G.Identification of oral candidosis, hairy leukoplakia and recurrent oral ulcers as distinct cases of immune reconstitution inflammatory syndrome. Int J STD AIDS. 2009 Apr;20(4):259-61 Kakabadze T, Rukhadze N, Mshvidobadze K, Lomtadze M, Kandelaki G.Oral lesions in HIV-positive patients in Georgia.Georgian Med News. 2008 Dec;(165):60-5. Carpio E, López V, Fardales V, Benítez I.Oral manifestations of HIV infection in adult patients from the province of Sancti Spiritus, Cuba.J Oral Pathol Med. 2009 Jan;38(1):126-31 Li ZC, Zhao Y, Dou ZH, Yu L, Wu H, Zhang FJ.[Clinical features of 66 children with acquired immunodeficienecy syndrome.] Zhongguo Dang Dai Er Ke Za Zhi. 2009 Feb;11(2):93-5 Sanjay Saraf. Textbook of Oral Pathology. In: Bacterial, Viral, Mycotic and Protozoal Disorders.1st ed.Delhi: Jaypee 2006;pp 103-7

27. Any Questions?

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